Drosophila rely primarily on innate immune responses to effectively combat a wide array of microbial pathogens. The hallmark of the Drosophila humoral immune response is the rapid production of AMPs (antimicrobial peptides) by the fat body, the insect homologue of the mammalian liver. Production of these AMPs is controlled at the level of transcription by two NF-kappaB (nuclear factor kappaB) signalling pathways. The Toll pathway is activated by fungal and many Gram-positive bacterial microbes, whereas the IMD (immune deficiency) pathway responds to Gram-negative bacteria and certain Gram-positive bacilli. In the present review, we discuss the mechanisms involved in bacterial recognition, in particular the differential recognition of various types of bacterial PGN (peptidoglycan) by different members of the PGRP (PGN recognition protein) family of receptors.